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PubMed1990

Clinical profile, therapeutic approach and outcome of gouty arthritis in northern India.

Thirty patients with gouty arthritis were studied over 3 years. The diagnosis was established with the help of polarised light microscopy. All the patients were males, with a median age of 45 years. They belonged to the middle or upper socio-economic class and were obese (mean body mass index 29.7). Chronic alcoholism, diabetes mellitus and hypertension were present in one patient each. No patient had symptomatic coronary artery disease. Although 6 patients had a history of renal colic, only one had gouty nephropathy with chronic renal failure. Six patients had a positive family history of gout. The disease involved mostly the joints of the lower extremity and podagra was observed in 70% of patients. Eight patients had tophi at various sites. There were 17 'over producers' and 13 'under excretors' of uric acid. The treatment consisted of patient education, symptomatic control with non steroidal anti-inflammatory drugs and/or colchicine and antihyperuricaemic therapy. The overproducers were treated with allopurinol while the under excretors were treated with [corrected] sulfinpyrazone. In general, there was a good response to therapy as indicated by lowering of serum uric acid and the number of painful episodes per year. The overall profile of the disease appears similar to that seen in the West.

Adult↗

PubMed1987

Antiplatelet therapy in thrombotic thrombocytopenic purpura.

The presence of platelet-fibrin microthrombotic occlusions in the arterioles and capillaries of involved tissues of patients with TTP has suggested a role for platelet aggregation in this disorder. Inhibitors of platelet aggregation have been reported to produce resolution of thrombocytopenia and clinical improvement in many instances. Failure of such agents to produce a clinical effect has been attributed to inadequate dose-duration, severity and extent of end organ/vascular involvement, long-term or secondary effects of the etiologic principal leading to patient deterioration and/or demise. On the other hand, the parallel use of several treatment modalities that themselves may produce clinical effect confounds the interpretation that anti-platelet agents alone may have been responsible for clinical improvement. Nonetheless, complete remission has been reported in a number of TTP patients when the combination ASA/dipyridamole was used alone or together with plasmapheresis, splenectomy, and/or other antiplatelet agents. The evidence for a beneficial clinical effect would seem strongest for the use of this combination early in the course of the disease. More limited and less conclusive has been the experience with sulfinpyrazone, with ticlopidine, and with intravenous PGI2 infusions in TTP. Reports of clear-cut benefit with each of these agents have been rare. Finally, serial dextran infusions have apparently produced amelioration of the clinical syndrome in certain individuals. Assessment of benefit of dextran infusions from retrospective series has been limited by antecedent use of splenectomy. The use of red cell and plasma infusions during splenectomy has been argued to provide some benefit. However, it is likely that dextran can produce definite responses in certain patients. Unfortunately, therapeutic efficacy has been judged from such anecdotal reports and retrospective series. No prospective controlled trials of any of these approaches are available.

Aspirin↗

PubMed1989

Observations with Rabenid in patients with locomotor disease.

By examining 139 patients suffering from locomotor diseases the author could observe the characteristic accompanying diseases as well as high uric acid level in 40 cases. She analyses the current opinions on hyperuricaemia and reports on her observations with uricosuric and antithrombotic coated Rabenid tablet (RG). She found sulfinpyrazone to be effective and valuable in the examined indication field.

Adult↗

PubMed1987

Anti-platelet agents reduce morphological changes of chronic hypoxic pulmonary hypertension.

The pathophysiologic mechanism by which chronic hypoxia causes pulmonary hypertension is unknown. If anti-platelet agents, or other pharmacologic interventions, altered the pulmonary vascular changes induced by hypoxia, information concerning the pathogenesis of the pulmonary hypertension or the potential therapeutic usefulness of the drugs might be obtained. In Study 1, rats exposed to chronic hypobaric hypoxia (PB = 520 mmHg) had a pulmonary arterial medial thickness of 6.7 +/- 0.6 mu compared to 4.1 +/- 0.2 mu* for control, normoxic rats (*p less than 0.05). Administration of dipyridamole (2mg/kg/day), or sulfinpyrazone (11 mg/kg/day) in the drinking water reduced the medial thickness to 5.0 +/- 0.3 mu* and 5.4 +/- 0.5 mu* respectively, thus suggesting the possible involvement of platelets in the response of the media to chronic hypoxia. In Study 2, hypoxic rats treated with the calcium blocker, flunarizine, were found to have less medial hypertrophy than a control group of hypoxic rats. This observation suggests that a decrease in transmembrane calcium flux may also reduce medial hypertrophy.

Animals↗

PubMed1985

Cyclosporine-associated lymphoproliferation, despite controlled cyclosporine blood concentrations, in a renal allograft recipient.

In a patient receiving sulfinpyrazone (Anturan, Geigy) an unusually high dose of cyclosporine (Cys) was required to maintain serum values in the range of 50-200 ng/ml. After eight months of 1300-1500 mg/day, the patient complained of increasing malaise and symptoms of cyclosporine side-effects. This clinical state was accompanied by splenomegaly and two monoclonal peaks in the gamma region on serum electrophoresis. Concomitantly, rising cytomegalovirus IgM titres, following by rising IgG titres, indicated a primary cytomegalovirus infection. This ominous biclonal proliferation markedly diminished during the subsequent six months, during which time the cyclosporine dose was minimised. He returned to good health, splenomegaly and monoclonal gamma globulin virtually disappearing. He remains well at 16 months post-transplantation.

Cyclosporins↗

PubMed1978

Platelet-suppressant therapy in patients with coronary artery disease.

Platelets may contribute to the pathogenesis of atherosclerosis and to the complications of coronary atherosclerosis, acute myocardial infarction, unstable angina, and sudden cardiac death. In addition, platelets may contribute to saphenous vein aortocoronary graft occlusion. Of 104 men with coronary artery disease, platelet survival (SURV) (chromium51 labeling) was shortened in 68% (3.1+/-0.03 days [average+/-SEM]; normal, 3.7+/-0.03 days; P greater than .001). Three platelet-suppressant drugs, sulfinpyrazone, clofibrate, and dipyridamole increased SURV. Saphenous vein graft occlusion was associated with shortened SURV. Of 36 men with occlusion of at least one graft, SURV was shortened in 35 (2.5+/-0.08 days), whereas in 19 with all grafts open, SURV was shortened in six (3.5+/-0.10 days; P less than .01). These drugs increased SURV (2.3 +/- 0.08 to 2.7 +/- 0.11 days; P less than 0.1) and were associated with improved graft patency (four of 32 grafts after initial bypass vs 30 of 34 grafts open after second operation).

Adult↗

PubMed1985

[Controversy on platelet-inhibiting drugs].

The only well established, clinically useful platelet inhibiting drug is aspirin, though the optimal dose is unknown. Experimental findings, the virtual absence of side effects and, so far, four clinical studies favour a dose of 100-300 mg per day. The majority of clinical studies, however, and particularly those involving patients with cerebrovascular diseases, have employed doses of aspirin of 1000-1200 mg per day. Aspirin reduces mortality and infarction rates in patients who have already had myocardial infarction by 0-30%. The efficacy of additional dipyridamol or of sulfinpyrazone is not proven either. So far the effects of aspirin in patients with unstable angina and in patients after aortocoronary bypass surgery are more favourable. The best evidenced indication for aspirin treatment is transient ischemic attacks and status post stroke. The beneficial effect of aspirin in these conditions may also extend to women. Additional dipyridamol is also useless in this condition.

Angina, Unstable↗

PubMed1985

Secondary prevention of myocardial infarction.

Aspirin, sulfinpyrazone and the combination of aspirin/dipyridamole, which inhibit some aspects of platelet function, have been evaluated in large-scale clinical trials in secondary prevention of myocardial infarction. The Persantine-Aspirin Reinfarction Study using dipyridamole, and Anturane Reinfarction Trial and Anturan Reinfarction Italian Study with sulphinpyrazone did not yield conclusive results. There have been five trials in which aspirin has been compared with a placebo. When the results were pooled, the outcome was consistent with a reduction during aspirin treatment of 5-10% in mortality and 20% in coronary event-rate. Whether this small benefit to an individual patient is worthwhile, and whether the effect of aspirin is influenced by coexistent beta-blocker treatment, is not clear.

Aspirin↗

PubMed1973

Platelets in hyperacute rejection of heterotopic cardiac allografts in presensitized dogs. An experimental study.

Experiments were carried out to determine whether platelet aggregation plays a primary role in cardiac allograft hyperacute rejection, as has been observed in renal allograft hyperacute rejection. Dogs were presensitized by multiple skin grafts before a cervical heterotopic cardiac allograft was placed. One group of dogs was treated with sulfinpyrazone, a platelet inhibitor, and another was not. In the majority of the untreated dogs, the cardiac transplants were rejected hyperacutely and showed, morphologically, platelet aggregation followed by vascular disruption. In the treated dogs, hyperacute rejection was prevented, but the cardiac transplants were later rejected by primary cellular rejection. These data and the results from the experiments of other researchers lead us to propose that platelets are the "effector" of hyperacute rejection.

Animals↗

PubMed1979

[Pharmacologic remobilization of hyperadhesive granulocytes: a new principle in "anti-inflammatory" therapy].

It is thought that the nonsteroidal anti-inflammatory drugs act through inhibition of cyclooxygenase (CO). The authors show that the pyrazolon derivatives phenylbutazone (P) and sulfinpyrazone (S) affect PMN function in a manner independent of CO inhibition. During inflammation PMN often show increased adhesiveness. Such adhesiveness can be provoked in vitro by high concentrations of chemotaxins. Preincubation (10--20 minutes) of platelet-free human PMN suspensions in heat-inactivated plasma with 100 micrograms P or S per ml completely abolished a submaximal adherence induction on Petri dishes from 4% adherent cells in the absence, to 23% in the presence, of 10(-7) M of the chemotaxin N-f-Met-Leu-Phe (FP). In vivo, premedication of rabbits with P or S prevented the FP-induced neutropenia, e.g. 10 mg/kg of S blocked a 5-minutes agranulocytosis. P and S also abrogated adherence-induced lysosomal enzyme release and FP-stimulated hexose monophosphate pathway (HMP) activity. FP-induced hyperadhesiveness impedes PMN locomotion. Preincubation of PMN with P or S reestablished random motility and allowed chemotactic migration toward activated C (as C5a) in spite of the presence of 'adhesive' concentrations of FP. The potent CO inhibitors indomethacin and aspirin had no effect on FP-induced adherence, enzyme release, neutropenia and HMP stimulation. In 3 selected patients with PMN hyperadhesiveness, correction of this adhesiveness by P paralleled clinical remission. It is concluded that P and S exert their antiinflammatory action at least in part by interfering with PMN hyperadhesiveness and lysosomal enzyme release. These effects are independent of the prostaglandin-thromboxane system, since other CO inhibitors are uneffective.

Cell Adhesion↗

PubMed1979

Is the antithrombotic activity of "antiplatelet" drugs based on protection of endothelium?

In only five "antiplatelet" agents has the antithrombotic activity been confirmed both clinically and experimentally. These include acetylsalicylic acid, dipyridamole, clofibrate, hydroxychloroquine and sulfinpyrazone. Whereas only acetylsalicylic acid has a demonstrable effect on platelet aggregation in doses usually applied, the effects of all remaining drugs are more easily explained by their influence on the vessel wall. This assumption is supported by the finding that all five drugs possess a stabilizing effect on endothelium in doses corresponding closely to the clinical dose range. The method based on counting detached endothelial cells in blood after a standard stimulus was used to demonstrate this effect.

Animals↗

PubMed1979

[Inhibitors of platelet aggregation in the therapy of arteriosclerosis obliterans].

The central role of the thrombocytes in the initial atherogenesis and the secondary formation of the thrombus on sclerotically changed walls of the vessels is the basis of all experiments to perform a primary or secondary prevention of the atherosclerosis with thrombocyte aggregation inhibitors. Of the numerous thrombocyte-inhibiting substances acetyl salicylic acid, dipyridamol and sulfinpyrazone proved most suitable for clinical purposes. Apparantly for methodical reasons experiments of a primary prevention of the atherosclerosis with aggregation inhibitors have hitherto not be performed. On the other hand, in numerous quantitatively very different studies on patients with manifest cerebral, coronary and peripheral arteriosclerosis the influencibility of the course of the disease was tested by thrombocyte inhibitors. Since correct prospective studies are connected with enormous organisational expenditure and must extend for a longer period many extensive examinations have not yet finished. In the present survey the hitherto existing reports from literature are critically summarized, taking into particular consideration the per ipheral angioorganopathies and first informations on an own study concerning the prophylaxis of the diabetic angiopathy with Micristin are given. The present state of knowledge allows the conclusion that the well founded theoretical concept is apparantly confirmed by practice. However, the successes observed could be statistically ascertained only in individual cases, so that at present a final estimation of the prophylactic value of these preparations is not yet possible.

Arteriosclerosis Obliterans↗

PubMed1977

The retired breeder rat as a new model for antiplatelet drug discovery.

Spontaneous circulating platelet aggregates were observed in male retired breeder rats but in nonbred males of the same age and strain. Fasting serum lipid, platelet serotonin, and platelet rich plasma cyclic guanosine monophosphate levels were similar in retired breeders and nonbred rats. The in vitro response of platelets from retired breeder and nonbred rats to adenosine diphosphate and collagen were also similar. Administration of prostaglandin E1 and antiplatelet drugs (acetylsalicylic acid, sulfinpyrazone, and dipyridamole) reduced the number of circulating platelet aggregates in the breeder rats. It was concluded that the retired breeder rat may be a useful model for identification of new anti-platelet drugs.

Animals↗

PubMed1983

[Role of antiplatelet agents in the prevention of cerebral ischemic accidents].

This is a critical review of controlled therapeutic trials concerned with the use of anti-platelet agents in the prevention of cerebral ischaemic accidents due to atherosclerosis (CIADA). Amongst the 4 substances studied in 9 trials, dipyridamole, clofibrate, sulfinpyrazone and aspirin, only aspirin at the dose of 1 g brought about a statistically significant reduction in the risk of cerebral infarction and death in patients who had suffered an initial transient or rapidly regressive cerebral ischaemic accident. Nevertheless, this preventive action was seen in only one of the 5 studies devoted to aspirin and was found only in men, in particular where there was no history of diabetes or myocardial infarction. Although encouraging, this result requires confirmation by other studies before any definite conclusion is drawn as to the efficacy of aspirin in the secondary prevention of CIADA.

Adult↗

PubMed1983

Spasmogenic properties of platelet-activating factor: evidence for a direct mechanism in the contractile response of pulmonary tissues.

Platelet-activating factor (1-O-alkyl-2-O-acetyl-sn-glycero-3-phosphocholine; PAF) induces a specific, dose-dependent contraction of guinea pig lung parenchymal strips with an ED50 value of 10(-9) M. The smooth muscle contractile activity of PAF in this system was not effected by the H1-blocking antihistamine, pyrilamine (10(-6) M), the prostaglandin synthesis inhibitors, indomethacin (10(-5) M), aspirin (10(-4) M), or sulfinpyrazone (5 X 10(-4) M), the leukotriene synthesis inhibitor, nordihydroguaiaretic acid (NDGA; 10(-5) M), the leukotriene antagonist FPL 55712 (10(-6) M) or the inhibitor of arachidonic acid metabolism, eicosatetraynoic acid (ETYA; 2 X 10(-5) M). The role of platelets in this system was also investigated. PAF-mediated contractions were not attenuated following platelet depletion using nitrogen mustard, nor were they augmented by the addition of exogenous platelets. Furthermore, isolated platelets incubated with PAF did not release stable substances spasmogenic for lung parenchymal strips. Finally, contractile activity of PAF was demonstrated in lung parenchymal strips from rats, a species whose platelets are insensitive to PAF at elevated concentrations. Taken together, these data show that PAF contracts smooth muscle of guinea pig lung parenchyma independently of endogenous histamine, arachidonic acid metabolites, or platelets trapped within the pulmonary vasculature. It is concluded, therefore, that PAF may act directly on contractile cells of the lung.

5,8,11,14-Eicosatetraynoic Acid↗

PubMed1981

Adrenochrome-induced coronary artery constriction in the rat heart.

Adrenochrome, an oxidation product of epinephrine, has been demonstrated to produce cardiotoxic effects. In this study, we have investigated whether this agent can alter coronary resistance in isolated rat hearts. Concentrations of adrenochrome from 1 to 1000 ng/ml increased coronary pressure in a dose- and time-dependent manner. The highest concentration produced a 3-fold elevation in pressure after a 1-hr perfusion. Myocardial contractile force decreased only with either 100 or 1000 ng/ml of adrenochrome and this effect was evident after substantial elevations in coronary pressure. The elevation in coronary pressure was significantly reduced by two calcium antagonists, verapamil and D-600. Furthermore, the degree of constriction by adrenochrome was dependent on the CaCl2 concentration in the perfusion medium. High concentrations of indomethacin or propranolol attenuated the degree of coronary pressure elevation, whereas acetylsalicylic acid and phenoxybenzamine were without effect. Sulfinpyrazone, which has been shown to reduce the arrhythmogenic action of adrenochrome in vivo, significantly reduced the coronary pressure increases. These results suggest that adrenochrome is a potent coronary constricting agent in the rat heart and its action is seemingly dependent on external Ca++ availability.

Adrenochrome↗

PubMed1981

Antiplatelet therapy.

Much new information has been gleaned about the morphology, biochemistry and function of platelets. The pathophysiology of atherosclerosis and thromboembolic disorders appears to be related to abnormal platelet function. Endothelial damage, thromboxane A2, Thrombin, adenosine diphospate and epinephrine may each promote platelet aggregation, whereas prostacyclin impairs aggregation. Aspirin, sulfinpyrazone and dipyridamole have been used as antiplatelet agents, and specific indications are being developed to guide their selection.

Anticoagulants↗

PubMed1981

[Study of platelet aggregation by the filtration pressure method (author's transl)].

Using Hornstra's "filter loop" technique, effects of prostaglandins and vasodilators on ADP-induced platelet aggregation were studied in anaesthetized dogs. ADP-induced platelet aggregation was observed as a transient, reversible elevation of pressure before filter. This pressure change was reproducible and dose-related. PGI2 and PGE1 suppressed the elevation of pressure induced by ADP and decreased the spontaneous elevation of pressure. Thus, it was reconfirmed that PGI2 and PGE1 not only suppressed ADP-induced platelet aggregation but also produced a disaggregation of aggregated platelets. AFter indomethacin, ADP-induced platelet aggregation was potentiated and sometimes became exceedingly protracted, indicating that anti-aggregatory prostaglandin was always present in the circulating blood. Close-injection of bradykinin did not suppress ADP-induced platelet aggregation, while intravenous injection did produce a suppression. After indomethacin, this inhibitory effect was greatly attenuated, indicating a release of anti-aggregatory prostaglandin (PGI2?) by bradykinin. Coronary vasodilators, such as dipyridamole and nifedipine did not inhibit ADP-induced platelet aggregation, nor did sulfinpyrazone. It is concluded that the "filter loop" technique is a useful method that allows aggregation and disaggregation reactions to be followed continuously and quantitatively in the blowing blood. The effects of drugs on platelet aggregation can be assessed in connection with hemodynamic changes such as blood pressure and heart rate induced by systemic administration of the drugs.

Adenosine Diphosphate↗